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AASLD Guidelines for Treatment of Chronic Hepatitis B

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AASLD Guidelines for Treatment of Chronic Hepatitis B PRACTICE GUIDELINE AASLD Guidelines for Treatment of Chronic Hepatitis B Norah A. Terrault,1 Natalie H. Bzowej,2 Kyong-Mi Chang,3 Jessica P. Hwang,4 Maureen M. Jonas,5 and M. Hassan Murad6 1. Should adults with immune active CHB be See Editorial on Page 31 treated with antiviral therapy to decrease liver- related complications? Objectives and Guiding Principles 2. Should adults with immune-tolerant infection be treated with antiviral therapy to decrease liver- Guiding Principles related complications? This document presents official recommendations of 3. Should antiviral therapy be discontinued in hepati- the American Association for the Study of Liver Diseases tis B e antigen (HBeAg)-positive persons who have (AASLD) on the treatment of chronic hepatitis B (CHB) developed HBeAg seroconversion on therapy? virus (HBV) infection in adults and children. Unlike pre- 4. Should antiviral therapy be discontinued in per- vious AASLD practice guidelines, this guideline was sons with HBeAg-negative infection with sus- developed in compliance with the Institute of Medicine tained HBV DNA suppression on therapy? standards for trustworthy practice guidelines and uses the 5. In HBV-monoinfected persons, does entecavir ther- Grading of Recommendation Assessment, Development apy, when compared to tenofovir therapy, have a and Evaluation (GRADE) approach.1 Multiple systematic different impact on renal and bone health? reviews of the literature were conducted to support the 6. Is there a benefit to adding a second antiviral agent recommendations in this practice guideline. An enhanced in persons with persistent low levels of viremia while understanding of this guideline will be obtained by read- being treated with either tenofovir or entecavir? ing the applicable portions of the systematic reviews. 7. Should persons with compensated cirrhosis and low This guideline focuses on using antiviral therapy in levels of viremia be treated with antiviral agents? chronic HBV infection and does not address other related 8. Should pregnant women who are hepatitis B sur- and important issues, such as screening, prevention, and face antigen (HBsAg) positive with high viral surveillance. For broader issues related to diagnosis, sur- load receive antiviral treatment in the third tri- veillance, and prevention as well as treatment in special mester to prevent perinatal transmission of HBV? populations (e.g., liver transplant recipients) that are not 9. Should children with HBeAg-positive CHB be addressed by this guideline, the previous AASLD guide- treated with antiviral therapy to decrease liver- line2 and recent World Health Organization (WHO) related complications? 3 guideline are excellent additional resources. Target Audience Objectives This guideline is intended primarily for health care Guideline developers from the AASLD formulated a professionals caring for patients with CHB. Addition- list of discrete questions that physicians are faced with ally, this guideline may assist policy makers in optimiz- in daily practice. These questions were: ing the care of individuals living with CHB. Abbreviations: AASLD, American Association for the Study of Liver Diseases; ALT, alanine aminotransferase; anti-HBe, antibody to HBeAg; anti-HBs, antibody to HBsAg; APRI, AST-to-platelet ratio index; AST, aspartate aminotransferase; cccDNA, covalently closed circular DNA; CHB, chronic hepatitis B; CI, confidence interval; GRADE, Grading of Recommendation Assessment, Development and Evaluation; HBV, hepatitis B virus; HCV, hepatitis C virus; HCC, hepatocellular carci- noma; HIV, human immunodeficiency virus; HDV, hepatitis delta virus; HBsAg, hepatitis B surface antigen; HBeAg, hepatitis B e antigen; IFN, interferon; NA, nucle- os(t)ide analog; Peg-IFN, pegylated interferon; RCT, randomized, controlled trial; RR, relative risk; ULNs, upper limits of normal; WHO, World Health Organization. From the 1University of California San Francisco, San Francisco, CA; 2Ochsner Medical Center, New Orleans, LA; 3Corporal Michael J. Crescenz VA Medical Center & University of Pennsylvania Perelman School of Medicine, Philadelphia, PA; 4The University of Texas MD Anderson Cancer Center, Houston, TX; 5Bos- ton Children’s Hospital, Harvard Medical School, Boston, MA; 6Mayo Clinic, Rochester, MN. Received August 24, 2015; accepted August 25, 2015. Additional Supporting Information may be found at onlinelibrary.wiley.com/doi/10.1002/hep.28156/suppinfo. The funding for the development of this Practice Guideline was provided by the American Association for the Study of Liver Diseases. This Practice Guideline was approved by the AASLD on August 1, 2015. This Practice Guideline published with accompanying Reviews by Lok et al., Jonas et al., and Brown et al. 261 262 TERRAULT ET AL. HEPATOLOGY, January 2016 Table 1. Phases of CHB Infection ALT HBV DNA HBeAg Liver Histology Immune-tolerant phase Normal Elevated, typically Positive Minimal inflammation and fibrosis >1 million IU/mL HBeAg-positive Elevated Elevated Positive Moderate-to-severe inflammation or fibrosis immune-active phase 20,000 IU/mL Inactive CHB phase Normal Low or undetectable Negative Minimal necroinflammation but variable fibrosis <2,000 IU/mL HBeAg-negative immune Elevated Elevated Negative Moderate-to-severe inflammation or fibrosis reactivation phase 2,000 IU/mL need for treatment. Of note, some persons will be in the Background “gray zones,” meaning that their HBV DNA and ALT Burden of Disease levels do not fall into the same phase. Longitudinal Globally, an estimated 240 million persons have follow-up of ALT and HBV DNA levels and/or assess- CHB with a varying prevalence geographically, highest ment of liver histology can serve to clarify the phase of in Africa and Asia.4 In the United States, the National infection. Health and Nutrition Examination Survey (1999 to i. Immune-tolerant phase: In this highly replicative/ 2008) identified approximately 704,000 adults with low inflammatory phase, HBV DNA levels are 5 CHB, but with adjustments for hepatitis B infection elevated, ALT levels are normal (<19 U/L for among foreign-born persons, the upper estimate of females and <30 U/L for males), and biopsies CHB in the United States may be as high as 2.2 are without signs of significant inflammation or 6 million. Globally, deaths from cirrhosis and hepatocel- fibrosis. The duration of this phase is highly vari- lular carcinoma (HCC) were estimated at 310,000 and able, but longest in those who are infected peri- 340,000 per year, respectively.7 To reduce the morbidity natally. With increasing age, there is an and mortality of CHB in the United States and world- increased likelihood of transitioning from wide, there is a need for continued efforts to identify immune-tolerant to the HBeAg-positive immune- infected individuals through targeted screening, prevent active phase. new infections through vaccination, and monitor and ii. HBeAg-positive immune-active phase: Elevated treat those at risk for complications of their CHB, ALT and HBV DNA levels in conjunction with including surveillance for HCC.8,9 liver injury characterize this phase. Median age of onset is 30 years among those infected at a young Natural History in Adults and Children age. The hallmark of transition from the HBeAg- CHB has been traditionally characterized into four positive immune-active to -inactive phases is phases (Table 1), reflecting the dynamic relationship HBeAg seroconversion. The rate of spontaneous between viral replication and evolution and the host seroconversion from HBeAg to antibody to HBeAg immune response. These phases are of variable duration (anti-HBe) is less than 2% per year in children and not every person infected with CHB will evolve younger than 3 years of age and increases during through all phases. Given the dynamic nature of CHB puberty and among adults to 8% and 12% per infection, serial monitoring of HBV DNA and alanine year, respectively. aminotransferase (ALT) levels is important to character- iii. Inactive CHB phase: In this phase, HBV DNA ize the phase of infection. A single ALT and HBV DNA levels are low or undetectable, ALT levels are nor- level are insufficient to assign phase of infection and/or mal, and anti-HBe is present. Liver histology Address reprint requests to: Norah Terrault, M.D., M.P.H., Division of Gastroenterology, University of California San Francisco, 513 Parnassus Avenue, S357, San Francisco, CA 94143-0538. E-mail: [email protected]; fax: 11-415-502-6714. Copyright VC 2015 by the American Association for the Study of Liver Diseases. View this article online at wileyonlinelibrary.com. DOI 10.1002/hep.28156 Potential conflict of interest: Dr. Jonas consults and received grants from Gilead. She received grants from Bristol-Myers Squibb and Roche. Dr. Chang advises Genentech, Alnylam, and Arbutus. Dr. Terrault consults for Bristol-Myers Squibb and received grants from Gilead. Dr. Bzowej received grants from Gilead, Synageva, and Ocera. HEPATOLOGY, Vol. 63, No. 1, 2016 TERRAULT ET AL. 263 Table 2. Host, Viral/Disease, and Environmental Factors region, and liver histology shows necroinflamma- Associated With Cirrhosis and HCC tion and fibrosis. Persons with HBeAg-negative Cirrhosis HCC CHB tend to have lower serum HBV DNA levels Host >40 years of age >40 years of age than those with HBeAg-positive CHB and are more Male sex Male sex likely to experience a fluctuating course. Immune compromised Immune compromised Positive family history Resolved CHB infection is defined by clearance of Born in Sub-Saharan Africa HBsAg with acquisition of antibody to HBsAg. Approx- Viral/ High serum HBV DNA Presence of cirrhosis disease (>2,000 IU/mL) High serum HBV DNA imately 0.5% of persons with inactive CHB will clear Elevated ALT levels (>2,000 IU/mL) HBsAg yearly; most will develop antibody to HBsAg Prolonged time to HBeAg Elevated ALT (anti-HBs). Low levels of HBV DNA are transiently seroconversion Prolonged time to HBeAg detected in the serum in the minority of persons achiev- Development of seroconversion 10,11 HBeAg-negative CHB Development of ing seroclearance. Clearance of HBsAg, whether Genotype C HBeAg-negative CHB spontaneous or after antiviral therapy, reduces risk of Genotype C hepatic decompensation and improves survival.
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